More Than mTOR? Novel Roles for MEK-ERK1/2 and FLNA in Tuberous Sclerosis Complex.
作者信息
Dulla Chris G
出版信息
Epilepsy Curr. 2015 Jul-Aug;15(4):221-2. doi: 10.5698/1535-7511-15.4.221.
Abstract
摘要
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本文引用的文献
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Cytoskeletal proteins in cortical development and disease: actin associated proteins in periventricular heterotopia.皮质发育与疾病中的细胞骨架蛋白：室管膜下异位中的肌动蛋白相关蛋白
Front Cell Neurosci. 2015 Apr 1;9:99. doi: 10.3389/fncel.2015.00099. eCollection 2015.
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MEK-ERK1/2-dependent FLNA overexpression promotes abnormal dendritic patterning in tuberous sclerosis independent of mTOR.MEK-ERK1/2依赖性的丝状肌动蛋白（FLNA）过表达促进结节性硬化症中异常树突模式形成，且不依赖于雷帕霉素靶蛋白（mTOR）。
Neuron. 2014 Oct 1;84(1):78-91. doi: 10.1016/j.neuron.2014.09.009.
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Reduced juvenile long-term depression in tuberous sclerosis complex is mitigated in adults by compensatory recruitment of mGluR5 and Erk signaling.结节性硬化症患者的青少年长期抑郁减少，这是由于 mGluR5 和 Erk 信号的代偿性募集在成年期得到缓解。
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Science. 2013 Jul 5;341(6141):1237758. doi: 10.1126/science.1237758.
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A circuitry and biochemical basis for tuberous sclerosis symptoms: from epilepsy to neurocognitive deficits.结节性硬化症症状的电路和生化基础：从癫痫到神经认知缺陷。
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Regulable neural progenitor-specific Tsc1 loss yields giant cells with organellar dysfunction in a model of tuberous sclerosis complex.调节性神经祖细胞特异性 Tsc1 缺失导致神经节苷脂贮积症模型中巨细胞的细胞器功能障碍。
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The tuberous sclerosis complex.结节性硬化症。
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